Protective Effects of Polydatin on Septic Lung Injury in Mice via Upregulation of HO-1

Li, Xiaohui; Gong, Xia; Zhang, Lili; Jiang, Rui; Li, Hongzhong; Wu, Mengjiao; Wan, Jingyuan

doi:10.1155/2013/354087

Cited by 39 publications

(34 citation statements)

References 43 publications

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“…In mouse CLP model, Cox-2 expression was previously shown to increase in the lungs of septic mice [66], [67], [68], in addition dual inhibition of Cox-2 and 5-LOX successfully attenuated lung injury, reduced MPO activity and improved survival of these mice [69]. As shown in several in vitro and in vivo models, pathogens induce Cox-2 expression via activated Toll like receptors (TLRs) [39], [40].…”

Section: Discussionmentioning

confidence: 99%

Lactobacillus rhamnosus GG and Bifidobacterium longum Attenuate Lung Injury and Inflammatory Response in Experimental Sepsis

et al. 2014

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IntroductionProbiotic use to prevent nosocomial gastrointestinal and potentially respiratory tract infections in critical care has shown great promise in recent clinical trials of adult and pediatric patients. Despite well-documented benefits of probiotic use in intestinal disorders, the potential for probiotic treatment to reduce lung injury following infection and shock has not been well explored.ObjectiveEvaluate if Lactobacillus rhamnosus GG (LGG) or Bifidobacterium longum (BL) treatment in a weanling mouse model of cecal ligation and puncture (CLP) peritonitis will protect against lung injury.Methods3 week-old FVB/N mice were orally gavaged with 200 µl of either LGG, BL or sterile water (vehicle) immediately prior to CLP. Mice were euthanized at 24 h. Lung injury was evaluated via histology and lung neutrophil infiltration was evaluated by myeloperoxidase (MPO) staining. mRNA levels of IL-6, TNF-α, MyD88, TLR-4, TLR-2, NFΚB (p50/p105) and Cox-2 in the lung analyzed via real-time PCR. TNF-α and IL-6 in lung was analyzed via ELISA.ResultsLGG and BL treatment significantly improved lung injury following experimental infection and sepsis and lung neutrophil infiltration was significantly lower than in untreated septic mice. Lung mRNA and protein levels of IL-6 and TNF-α and gene expression of Cox-2 were also significantly reduced in mice receiving LGG or BL treatment. Gene expression of TLR-2, MyD88 and NFΚB (p50/p105) was significantly increased in septic mice compared to shams and decreased in the lung of mice receiving LGG or BL while TLR-4 levels remained unchanged.ConclusionsTreatment with LGG and BL can reduce lung injury following experimental infection and sepsis and is associated with reduced lung inflammatory cell infiltrate and decreased markers of lung inflammatory response. Probiotic therapy may be a promising intervention to improve clinical lung injury following systemic infection and sepsis.

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Section: Discussionmentioning

confidence: 99%

Lactobacillus rhamnosus GG and Bifidobacterium longum Attenuate Lung Injury and Inflammatory Response in Experimental Sepsis

et al. 2014

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“…However, they decreased with PD treatment, possibly because of the anti-inflammatory actions of PD brought about by the decrease in nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) expression [16,27].…”

Section: Discussionmentioning

confidence: 99%

Polydatin: a new therapeutic agent against multiorgan dysfunction

Zeng

Chen

et al. 2015

Journal of Surgical Research

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“…Moreover, the in vitro and in vivo influence of PD on inflammatory processes and apoptosis has been demonstrated efficiently in several models. 25,26,[29][30][31][32][33] Since inflammatory response and apoptosis play key roles in the pathogenesis of burn-induced lung injury and PD has potential anti-inflammatory and anti-apoptosis effects, we hypothesized that PD may provide protection against burn-induced lung injury.…”

Section: Introductionmentioning

confidence: 99%

Protective Effect of Polydatin Against Burn-Induced Lung Injury in Rats

Cai

Zeng

et al. 2014

Respir Care

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INTRODUCTION: Polydatin (PD) has anti-inflammatory and anti-apoptotic effects in ischemicreperfusion injury. Moreover, inflammatory responses and apoptosis play a role in the development of burn-induced lung injuries. Based on these findings, in this study we investigated the hypothesis that PD can ameliorate lung injury induced by extensive burns via reduction of inflammation and apoptosis. METHODS: Rats were subjected to 30% total body surface area burn injury followed by resuscitation. The treatment group received 45 mg/kg PD, and the burn group received the same amount of normal saline solution. No burn injury was inflicted in the sham group. Microvascular permeability, interstitial edema, neutrophil recruitment, and histopathological changes were detected by measuring Evans blue concentration, wet-to-dry lung weight ratio (W/D), myeloperoxidase (MPO) activity, and hematoxylin and eosin staining, respectively. To investigate the mechanism of action of PD, enzyme-linked immunosorbent assay, cell counting, terminal deoxyribonucleotidyl transferase-mediated deoxyuridine 5-triphosphate-digoxigenin nick end labeling (TUNEL) staining, fluorometric assay, and Western blot were used for assessing levels of inflammatory cytokines (tumor necrosis factor alpha, interleukin [IL]-1␤, and IL-6), total number of cells, and concentration of polymorphonuclear leukocytes (PMNs) in bronchoalveolar lavage fluid (BALF), the number of apoptotic cells, caspase-3 activity, and apoptosis-related proteins including Bax and Bcl-xl, respectively. RESULTS: Burn-injury rats exhibited significant lung injury characterized by the deterioration of histopathological characteristics, pulmonary microvascular hyperpermeability, and a high W/D, which were attenuated by PD (P ‫؍‬ .007 for permeability, P ‫؍‬ .004 for W/D). PD inhibited the burn-induced inflammatory response, as evidenced by the down-regulation of lung MPO activity (P ‫؍‬ .008), total number of cells, PMN concentration in BALF, and the local and systemic levels of the pro-inflammatory cytokines examined. Moreover, PD treatment dramatically prevented burn-induced pulmonary cell apoptosis in lungs, as reflected by the decrease in the number of TUNEL-positive cells (P ‫؍‬ .002) and changes in Bax, Bcl-xl, and caspase-3 activity (P ‫؍‬ .03). CONCLUSIONS: PD ameliorates burn-induced lung injury via its anti-inflammatory and anti-apoptotic effects, and PD treatment may therefore serve as a potential therapeutic target for the treatment of critical burn injuries.

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Protective Effects of Polydatin on Septic Lung Injury in Mice via Upregulation of HO-1

Cited by 39 publications

References 43 publications

Lactobacillus rhamnosus GG and Bifidobacterium longum Attenuate Lung Injury and Inflammatory Response in Experimental Sepsis

Lactobacillus rhamnosus GG and Bifidobacterium longum Attenuate Lung Injury and Inflammatory Response in Experimental Sepsis

Polydatin: a new therapeutic agent against multiorgan dysfunction

Protective Effect of Polydatin Against Burn-Induced Lung Injury in Rats

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